Overview:

 

Pathophysiology
Consultation Overview
Key Drivers
Treatment Priorities
Red Flags
Treatment Recommendations
Supportive Programs
Diet and Lifestyle Recommendations
Clinical Investigation and Pathology
Pharmaceutical Treatments
Footnotes
References

Pathophysiology:

• The thyroid is a master gland that produces hormones that regulate the metabolic processes of many of the body’s tissues including the heart, liver, kidney and muscles.
• Thyrotropin releasing hormone (TRH) produced by the hypothalamus, stimulates the production and release of thyroid stimulating hormone (TSH) by the pituitary. TSH promotes hormonal secretion, 85% to 90% of which is thyroxine (T4), with the remaining 10% to15% being active thyroid hormone, triiodothyronine (T3). T4 is part of a self-regulatory negative feedback loop, which reduces hypothalamic production of TRH and importantly, pituitary production of TSH.^[i],[ii]
• Hypothyroidism occurs when the thyroid gland produces too little thyroid hormone, when there is decreased conversion from T4 to T3, when there is an overproduction of reverse T3 (rT3), or when the body is not efficiently using thyroid hormone.
• Disturbances in any of these can increase TSH production with subsequent production of additional thyroid tissue and goitre formation, in an attempt to produce sufficient thyroid hormones.
• Hashimoto’s thyroiditis is a form of autoimmune hypothyroidism that occurs when antibodies attack the tissue in the thyroid gland, causing reduced thyroid hormone production.
• Euthyroid sick syndrome occurs during episodes of illness including systemic illness, fasting/starvation, major operation, and numerous additional health conditions.^[iii] The main feature of this syndrome is a fall in fT3 levels with normal TSH.
• Post-therapeutic hypothyroidism results from the treatment of hyperthyroidism with radioactive iodine or surgical removal of part or all of the thyroid gland. The treatment can leave the patient's thyroid unable to produce sufficient amounts of thyroid hormone.

Consultation Overview:

 

Identify Risk Factors

In Clinic Investigations- Refer to Key Drivers and the Clinical Investigation and Pathology sections below for further guidelines:

• Patient to perform a basal body temperature test at home.
• Examine the thyroid gland.
• Assess cardiovascular risk, as outlined in red flags section. Refer patient to a General Practitioner if suspected.
• Assess patient stress via the Metagenics Mood and Stress Questionnaire.
• Investigate possibility of pregnancy. Refer patient to a General Practitioner or Obstetrician where indicated.
• Assess for menstrual cycle irregularities and signs of oestrogen excess.
• Establish if patient has had significant exposure to environmental toxicants.
• For patients 65+ years, screen for osteopenia/osteoporosis.
• Omega-3 Index Test: Low omega-3 index is associated with increased inflammation.
• Assess Achilles deep tendon reflex contraction and relaxation time.

Pathology Investigations- Refer to Key Drivers and the Clinical Investigation and Pathology sections below for further guidelines:

• Test thyroid function: Refer patient for external laboratory testing or to a General Practitioner for assessment of serum TSH, free T4 (fT4) and fT3. For comprehensive assessment, consider rT3.
• Screen for inflammatory markers where indicated: Thyroid autoantibodies, erythrocyte sedimentation rate (ESR) and High-sensitivity C-reactive protein (hs-CRP).
• Screen for comorbidities where indicated, including dyslipidaemia, insulin resistance/blood glucose dysregulation and pernicious anaemia.

 

Identify Signs of Hypothyroidism

Fatigue Constipation Depression Dry hair and skin Hair loss Sensitivity to cold/cold intolerance Swelling of the thyroid gland Cognitive impairment

Hoarseness of voice Bradycardia Hypertension (diastolic) Unexplained weight gain/difficulty losing weight Muscle cramps and weakness Constipation Puffy eyes Elevated low-density lipoprotein (LDL) cholesterol

 

Key Drivers:

• Nutritional deficiencies: Iodine, selenium, vitamins A and E, are required for optimal thyroid function. Additionally, low levels of vitamin D are associated with increased thyroid autoimmunity;
• Inflammation: Hypothyroidism is associated with increased inflammatory markers including low omega-3 index, which is associated with reduced production of specialised pro-resolving mediators. Elevated tumour necrosis factor alpha (TNF-α) has also been found to decrease serum T3 and increases rT3, while elevated IL-6 suppresses T3 generation by deiodinases, D1 and D2. Additionally, subclinical hypothyroidism is associated with increased CRP and ESR^[iv];
• Oxidative stress: Inhibits thyroid function and peripheral conversion of thyroid hormones. Oxidative stress within the thyroid gland itself inhibits iodide uptake and induces DNA damage and apoptosis of thyroid cells;
• Stress: Suppresses TSH and decreases peripheral conversion of T4 to T3.  Increased cortisol encourages conversion of T4 to rT3, decreasing fT3;
• Gastrointestinal dysfunction: Gut dysbiosis is associated with loss of immune tolerance and the generation of self-antigens by post-translational modification of proteins, lipopolysaccharide (LPS)-induced Toll-like receptor 4 activation, induction of T helper 1 (Th1) to Th2 cell shift and activation of immune responses in the gut, and breach of tight junction integrity resulting in a leaky gut barrier.^[v] Additionally, hypothyroidism is a risk factor for small intestinal bacteria overgrowth (SIBO) development, due to intestinal motor dysfunction (decreased transit time), which reduces the ability of the small bowel to clear luminal bacteria^[vi];
• Coeliac disease: High prevalence of autoimmune thyroiditis among patients with coeliac;
• Oestrogen excess: Oestradiol decreases sodium-iodide symporter gene expression, reducing iodine uptake. Oestrogen also increases thyroid-binding globulin, reducing free thyroid hormones^[vii],[viii];
• Environmental toxicants: Dioxin, organochlorine, polychlorinated biphenyls, perfluoroalkyl acids, heavy metals, polybrominated biphenyls, and insecticides/herbicides/fungicides may act via two mechanisms; by directly disrupting thyroid function (altering TSH, T4 and T3) and/or by disrupting the immune system with subsequent triggering of autoimmune thyroid disease^[ix];
• Aggressive caloric restriction (>20%): Reduces total and free T3, and reduces peripheral conversion of T4 to T3^[x];
• Stealth infections: Viral and bacterial infections are associated with triggering of autoimmune thyroiditis in susceptible humans via two proposed mechanisms; molecular mimicry, which occurs when foreign antigens resemble self-antigens, and bystander activation, which triggers auto-reactive B cells and T cells;
• Spontaneous overt hypothyroidism occurs in 1% to 2% population.^[xi]

Figure 1: Factors that influence thyroid dysfunction.

Treatment Priorities

• Ensure precursor nutrients (tyrosine, iodine) and cofactors (selenium, zinc) for thyroid hormone production and conversion are nutrient replete.
• Support antioxidant and anti-inflammatory pathways to protect the thyroid gland from damage caused by oxidative stress and inflammation.
• Minimise exposure/correct drivers of thyroid disease, including chronic stress, gastrointestinal dysbiosis or exposure to environmental toxins.
• Determine autoimmune involvement via case taking of infectious/immune history and screen for thyroid autoantibodies where indicated.
• Monitor thyroid function via signs and symptoms, and use pathology testing where indicated
• Monitor patient’s adherence to dietary, lifestyle and supplementary recommendations.

 

Red Flags:

• Cardiovascular Disease (CVD): Hypothyroidism is associated with higher risks of myocardial infarction, and both overt hypothyroidism and subclinical hypothyroidism is associated with a higher risk of ischemic heart disease and cardiac mortality. Low thyroid function leads to elevated triglycerides and dyslipidaemia, diastolic hypertension, insulin resistance and metabolic syndrome, and endothelial dysfunction.^[xii],[xiii] Screen patient using the Cardiovascular Risk Assessment patient form. Monitor blood pressure and refer patient for pathology testing, including lipid profile, ESR, CRP, and fasting blood glucose. Refer patient to a General Practitioner for assessment if CVD is suspected.
• Pregnancy: A state of increased thyroid hormone demand. Accordingly, serum total T4 and T3 concentrations increase to approximately 150% of non-pregnant values.^[xiv] Elevations in TSH increase the risk of gestational diabetes, gestational hypertension and pre-eclampsia, preterm delivery, miscarriage and foetal death. Monitor TSH levels every four to six weeks during the first trimester and at least once in the subsequent trimesters.
• Infertility, ovulatory failure and/or recurrent miscarriages: Subclinical and overt hypothyroidism is associated with reproductive dysfunction, reducing the likelihood of pregnancy and increasing rates of miscarriage.^[xv]  Evaluate menstrual health and fertility using handouts, Monitoring Menstrual Cycle Signs, Menstrual Health Chart, and Fertility Awareness Chart. Support and stabilise thyroid function prior to conception.
• Pernicious anaemia: Autoimmune thyroid disease is the most common comorbidity of pernicious anaemia. Screen patients with autoimmune thyroid disease for vitamin B12 deficiency, and patients with pernicious anaemia for thyroid autoantibodies.^[xvi]
• Osteoporosis: High TSH levels, as seen in hypothyroidism, have been shown to directly affect bone metabolism through inhibition of osteoclast formation and survival, osteoblast differentiation and expression of collagen type 1.^[xvii] Patients 65 years of age and over are at an increased risk. Assess calcium and vitamin D levels, and refer patient for bone density analysis (dual energy X-ray absorption) and pathology investigation to measure bone turnover markers, C-terminal telopeptide of type 1 collagen (CTX) for bone resorption, and procollagen type 1 N propeptide (P1NP) for bone formation.^[xviii]

Treatment Recommendations

Core Recommendations

Lycium Hypothyroid Support

Loading dose: 2 tablets twice daily with food 

Maintenance dose: 1 tablet twice daily with food

The combination of herbs and nutrients provides multiple benefits for thyroid health including enhanced thyroid hormone production, antioxidant protection of thyroid tissue and adaptogenic support.

Mechanism of Action/Clinical Research:

• Withania has been shown to directly induce thyroid hormone release at the glandular level, enhance the conversion of T4 to T3, and to modulate levels of glucocorticoids.^[xix]
  • A randomised, double-blind, placebo-controlled trial involving 50 participants with subclinical hypothyroidism were prescribed 600 mg/d of withania for eight weeks, with results demonstrating statistically significant improvements in TSH, T3 and T4 levels.^[xx]
• Iodine is an essential cofactor for the production of thyroid hormones. T4, the prohormone, has four iodine molecules, and is converted to the active T3 by the removal of one of these iodines by deiodinase enzymes.^[xxi]
• Selenium is involved in the metabolism of iodine. Iodothyronine deiodinases enzymes, responsible for the activation of thyroid hormones, contain selenocysteine.^[xxii]
• Zinc is required in the cysteine residues of thyroid transcription factors and to facilitate the release of retinol-binding protein, which plays a central role in T4 to T3 conversion.^[xxiii]
• Vitamin A is required for peripheral metabolism of thyroid hormones and the conversion of T4 to T3 through induction of 5’-deiodinase in the liver and thyroid.^[xxiv] It is also required for the expression of T3 nuclear receptors.
• Vitamin E is important for the conversion of T4 to T3, supporting the function of iodothyronine 5’-deiodinase.^[xxv]

 

Mental and Physical Energy Powder

Dosage: 1 level scoop twice daily with food

Contains key ingredients that enhance energy production for those who experience fatigue due to impaired thyroid function.

Mechanism of Action/Clinical Research:

• Tyrosine is essential for the production of thyroxine. It undergoes iodination to produce T3 and T4.^[xxvi]
• Contains iodine, selenium and zinc, required for the synthesis of thyroid hormones (see above).
• Magnesium,^[xxvii] B vitamins^{[xxviii],[xxix],[xxx]} and carnitine^[xxxi] all play significant roles in energy production and the process of oxidative phosphorylation to form adenosine triphosphate (ATP), thus benefiting symptoms of fatigue.
• Four g/d of carnitine has been shown to reduce both physical and mental fatigue in a randomised, double-blind, clinical trial involving 96 subjects prescribed Acetyl-L-carnitine for 180 days.^[xxxii]

Additional Considerations

 

If with low iodine:

Iodine for Thyroid Health and Pregnancy Support

Dosage: 3 drops daily in water

Liquid iodine to replenish iodine levels and support thyroid gland health and function.

Mechanism of Action/Clinical Research:

• T4 and T3 are iodine-containing molecules. The conversion of T4 to T3 is accomplished by the removal of one iodine molecule by enzyme, 5’-deiodinase.^[xxxiii]
  • Taking 150 µg/d of potassium iodide in combination with thyroxine for 12 months has been shown to reduce nodule volume by 17.3%, versus 7.3% in the group using thyroxine alone.^[xxxiv]

 

If diagnosed with Hashimoto’s thyroiditis and/or presence of other autoimmune condition:

BCM-95™ Turmeric & Devil's Claw to Treat Chronic Inflammation

Dosage: Acute dose: 3 capsules twice daily, reducing to the maintenance dose of 1 capsule morning and two capsules evening, once symptoms have improved.

A combination of herbs to reduce production of inflammatory mediators at multiple points of the inflammatory cascade. If left untreated, autoimmune-associated inflammation can damage thyroid gland tissue, subsequently impacting the production of thyroid hormones.

Mechanism of Action/Clinical Research:

• Curcumin has broad anti-inflammatory effects, decreasing many inflammatory mediators including phospholipase, lipoxygenase (LOX), cyclooxygenase–2 (COX-2), leukotrienes (LTs), thromboxane, prostaglandins (PGs), nitric oxide (NO), collagenase, elastase, hyaluronidase, monocyte chemoattractant protein-1, interferon-inducible protein, TNF-α, and interleukin-12 (IL-12).^{[xxxv],[xxxvi]}
• Boswellia inhibits the cartilage-degrading enzyme, Matrix metalloproteinase-3 (MMP-3), while also preventing the decrease of glycosaminoglycan levels, which are essential for tissue repair.^{[xxxvii],[xxxviii]}

 

Lactobacillus paracasei LP-33^® and Lactobacillus rhamnosus (LGG^®) for Immune Control

Dosage: 1 capsule daily.

Clinically trialled probiotic strains to restore immune control and moderate over-active immune responses, which may be contributing to autoimmune thyroiditis.

Mechanism of Action/Clinical Research:

• Lactobacillus paracasei LP-33^® and Lactobacillus rhamnosus (LGG^®) have been shown to induce T regulatory cell production, which provides immunoregulatory support (Th1 and Th2 cytokine balance) and dampens inflammation in autoimmune disorders.^[xxxix],[xl]

 

Specialised Pro-Resolving Mediators^[1]

Specialised Pro-resolving Mediators (SPMs) to promote resolution, reduce pain, encourage the clearance of pathogens and mitigate pathological inflammation, without immunosuppression. In doing so, SPMs address inflammation, which is a major contributor to autoimmune thyroiditis.

Mechanism of Action/Clinical Research:

• SPMs encourage resolution by regulating macrophage polarisation: M1 macrophages, which are proinflammatory, and M2 macrophages, which inhibit polymorphonuclear neutrophils (PMNs) and promote efferocytosis, tissue repair, and resolution. SPMs trigger the switch from the M1 to the M2 phenotype, therefore reducing inflammation and tissue damage, and promoting resolution.^[xli]

 

Vitamin D3

Dosage: 1 capsules (1000 IU) daily

Vitamin D plays and important role in immune modulation and control of inflammation, to benefit immune function in autoimmune thyroid disease.

Mechanism of Action/Clinical Research:

• Vitamin D deficiency has been shown to result in an increased incidence of autoimmune diseases.^[xlii]
• Vitamin D regulates T helper cell and dendritic cell function and induces regulatory T cells, resulting in a decrease in Th1-driven autoimmune responses and development of self-tolerance.^[xliii]

For elevated triglycerides:

High Purity, Low Reflux, Concentrated Fish Oil Liquid or Capsules

Dosage: 4.2 mL (1 tsp) daily or 2 capsules twice daily.

Omega-3 essential fatty acids (EFAs) to reduce inflammation and support cardiovascular health by maintaining healthy lipid profiles, blood pressure and protecting arteries.

Mechanism of Action/Clinical Research:

• Eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) exert atheroprotective functions by promoting intracellular catabolism of apolipoprotein B-100 (ApoB-100) containing lipoproteins, suppressing hepatic apoB production, stimulating plasma triglyceride clearance via lipoprotein lipase, increasing the very low-density lipoprotein (VLDL) to LDL conversion rate, reducing LDL synthesis and attenuating postprandial lipaemia.^[li]
• In a randomised, placebo-controlled study involving 138 healthy males, 2.6 grams of EPA and DHA was shown to reduce triglyceride levels by 14%. The study indicated that there was a direct correlation between increased dosage and improved results.^[lii]

 

For elevated total cholesterol and/or LDL and ApoB:

Antioxidant Cholesterol Support Complex

Dosage: 1 capsule at night.

A proprietary blend of citrus flavonoids (polymethoxyflavones, PMFs) and tocotrienols (natural isoforms of vitamin E) to reduce cholesterol synthesis and beneficially support cardiovascular health.

Mechanism of Action/Clinical Research:

• PMFs reduce ApoB secretion and subsequent LDL synthesis in the liver, while also increase LDL-receptor synthesis for increased hepatic LDL clearance. In addition, PMFs mildly inhibit the activity of hepatic HMG-CoA reductase.^[liii]
• Tocotrienols inhibit LDL oxidation via antioxidant effects, decrease LDL levels via up-regulating LDL receptor expression, increase cholesterol clearance, and inhibit HMG-CoA reductase synthesis.^[liv]

 

If inflammation is present (elevated ESR and/or hs-CRP):

BCM-95™ Turmeric & Devil's Claw to Treat Chronic Inflammation

Dosage: Acute dose: 3 capsules twice daily, reducing to the maintenance dose of 1 capsule morning and two capsules evening, once symptoms have improved.

A combination of herbs to reduce production of inflammatory mediators at multiple points of the inflammatory cascade, benefiting chronic inflammatory conditions including hypothyroidism.

Mechanism of Action:

• Curcumin has broad anti-inflammatory effects, decreasing many inflammatory mediators including phospholipase, lipoxygenase (LOX), cyclooxygenase–2 (COX-2), leukotrienes (LTs), thromboxane, prostaglandins (PGs), nitric oxide (NO), collagenase, elastase, hyaluronidase, monocyte chemoattractant protein-1, interferon-inducible protein, TNF-α, and interleukin-12 (IL-12).^[lv],[lvi]
• Boswellia inhibits the cartilage-degrading enzyme, Matrix metalloproteinase-3 (MMP-3), while also preventing the decrease of glycosaminoglycan levels, which are essential for tissue repair.^{[lvii],[lviii]}

Specialised Pro-Resolving Mediators^[2]

Dosage: 1 capsule daily

Specialised Pro-resolving Mediators (SPMs) to promote resolution, reduce pain, encourage the clearance of pathogens and mitigate pathological inflammation, without immunosuppression. SPMs reduce production of inflammatory mediators associated with hypothyroidism.

Mechanism of Action:

• SPMs encourage resolution by regulating macrophage polarisation: M1 macrophages, which are proinflammatory, and M2 macrophages, which inhibit polymorphonuclear neutrophils (PMNs) and promote efferocytosis, tissue repair, and resolution. SPMs trigger the switch from the M1 to the M2 phenotype, therefore reducing inflammation and tissue damage, and promoting resolution.^[lix]

 

If patient presents with weight gain/difficulty losing weight or cardiovascular presentations:

Refer to the Metagenics Shake It Practitioner Weight Management Program under Supportive Programs

 

If patient presents with dysbiosis or additional gastrointestinal symptoms:

Refer to the Metagenics Clinical Detoxification Program under Supportive Programs

 

Supportive Programs

The Metagenics Shake It Practitioner Weight Management Program is designed to help patients comfortably transition from a hypercaloric diet to a hypocaloric diet, facilitating sustainable weight loss while also improving insulin sensitivity and optimising metabolic function. Given the association between hypothyroidism and cardiovascular disease, addressing any underlying metabolic drivers may improve thyroid function and associated symptoms.

Reduced exposure to environmental and endogenous toxins supports optimal thyroid function. The Metagenics Clinical Detoxification Program is designed to reduce toxic burden, increase toxin resilience and improve the efficiency of waste elimination.

 

Diet and Lifestyle Recommendations

Diet:

• Goitrogens such as sulphur-containing thioamides found in brassica vegetables including cabbage, broccoli and Brussels sprouts could impair the binding of iodine to thyroglobulin and prevent oxidation of iodide by thyroid iodide peroxidase.^[lx] Avoid consumption in large amounts.
• Foods containing goitrogenic cyanoglucosides, such as sweet potato and maize, release thiocyanate that competes with iodide, blocking its uptake by the thyroid.^[lxi]
• Adherence to a gluten-free diet has been shown to reduce anti-thyroid peroxidase antibodies (TPO-Ab).^[lxii]

Lifestyle:

Physical activity guidelines:

• Engage in 2.5 to 5 hours of moderate intensity physical activity or 1.25 to 2.5 hours of vigorous intensity physical activity, or an equivalent combination each week.
• Perform muscle strengthening/resistance training activities on at least two days each week.

Clinical Investigation and Pathology

 

Clinical Screening	Rationale
Basal Body Temperature	Using a digital thermometer, take temperature under the tongue on waking (before getting out of bed), preferably at the same time each day. Record temperature on Basal Body Temperature Tracker for at least four consecutive mornings, with an average taken of the readings. Normal reading: 36.5-37.0ºC Low readings (below 36.5ºC ) have been associated with underactive thyroid.
Examination of the Thyroid Gland	Clinical examination of the thyroid gland, combined with signs and symptoms, increases the accuracy of determining thyroid abnormality. Refer to Figure 2 for examination guidelines.
Achilles Reflex Time (Wolman Sign)	An alteration in the relaxation phase of deep tendon reflexes has been established as a characteristic clinical sign of hypothyroidism. Over 75% of hypothyroid patients display significantly prolonged contraction and relaxation phases of the Achilles reflexes. The basis for these changes may relate to the ability of thyroid hormone to regulate the sarcoplasmic reticulum calcium-activated ATPase. Delays in relaxation time in patients with hypothyroidism appears to be proportional to the level of thyroid hormone deficiency. Examples of delayed Achilles reflex presentations include: -       Woltman Sign Video -       Short Clinical Case: Woltman’s Sign of Hypothyroidism
Blood Pressure	Optimal reading: under 120/80 mmHg Normal to high: over 120/80 mmHg and up to 139/89 mmHg High: over 140/90 mmHg
Omega-3 Index Test	A validated test that measures red blood cell (RBC) EPA and DHA status. An Omega-3 Index in the desirable range of 8%-12% is an indicator of better overall health.

 

Figure 2: Examination of the thyroid gland.^[lxiii]

Pathology Testing	Ideal Reference Range	Rationale
Serum TSH	Ideal range: 0.4 to 2.0 mlU/L Subclinical hypothyroid: 2.0 to 4.0 mlU/L Overt hypothyroid: <4.0 mlU/L   Ideal range for preconception/pregnancy- Preconception: <2.5 mlU/L First trimester: 0.1 to 2.5 mlU/L Second trimester: 0.2 to 3.0 mlU/L Third trimester: 0.3 to 3.0 mlU/L	Currently, TSH concentration is the most reliable indicator of thyroid status at the tissue level.
Serum fT4	10 to 25 pmo/L	Considered to provide a reliable indication of true thyroid function.
Serum fT3	4 to 8 pmol/L	Performed as part of a more comprehensive evaluation of thyroid function.
rT3	Reference range: 140 to 540 pmol/L Ideal range: <240 pmol/L	Reverse T3 may help maintaining thyroid hormone homeostasis. Elevations have been observed in patients with hypothyroidism
TPO-Ab	Ideal range: <50 IU/mL Increased risk of thyroid dysfunction: 50 to 100 IU/mL	Elevations correlate with changes in the thyroid gland, which may reflect inflammation and tissue destruction. TPO-A is the most sensitive thyroid antibody test for assessing autoimmune hypothyroidism.
Thyroglobulin antibodies (TgAb)	Reference range: <4 IU/mL Ideal range: <1IU/mL	Often raised in autoimmune hypothyroidism.
ESR	Female: 17-50 years: 3 to 12 mm/hr >50 years: 5 to 20 mm/hr Male: 17-50 years: 1 to 10 mm/hr >50 years: 2 to 15 mm/hr	Raised ESR may be indicative of acute inflammation.
Hs-CRP	Normal value <10 mg/L However, ideal is <1 mg/L	Raised hs-CRP may be indicative of chronic inflammation.
Lipid profile	Total cholesterol <5.5 mmol/L HDL >1.00 mmol/L LDL <3.5 mmol/L Tryglycerides <2.0 mmol/L	Metabolic presentations such as dyslipidaemia are closely related to hypothyroidism, placing patients at increased risk of developing cardiovascular disease.
Blood glucose	Fasting plasma glucose: 3.5 to 6.0 mmol/L Random glucose: 3.5 to 9.0 mmol/L	Metabolic presentations including insulin resistance/blood glucose dysregulation are closely related to hypothyroidism.
Vitamin B12	Normal levels in adults and children: 120-680 pmol/L.	Additional driver of fatigue, and ruling out pernicious anaemia.
Iron Studies	Serum Fe: 14 to 30 µmol/L Total iron binding capacity: 45 to 80 µmol/L % Transferrin saturation: Female: 20 to 55%, Male: 20 to 60% Ferritin: 20 to 250 µg/L	Additional driver of fatigue, and ruling out pernicious anaemia.
Vitamin D	At least 50 nmol/L at end of winter Between 60 to 70 nmol/L during summer.	Deficiency is associated with Hashimoto’s thyroiditis.
CTX (bone resorption) P1NP (bone formation)	Refer to laboratory ranges	A high level of one or more bone markers in urine and/or blood suggests an increased rate of resorption and/or formation of bone, but it does not indicate the cause
Coeliac serology	Transglutaminase (tTG) IgA:* Gliadin Antibody IgA:* Gliadin Antibody IgG:*   *Ranges vary depending on testing methods (i.e. blood spot vs. blood draw). Refer to specific ranges provided by testing laboratory.	Serologic testing for coeliac disease consists of tissue Transglutaminase (tTG) and deamidated gliadin antibody tests. In practice, both tests have >85% sensitivity and >90% specificity. Diagnosis for coeliac disease requires affirmative small bowel tissue biopsy.

Pharmaceutical Treatments:

• Thyroxine/Levothyroxine: T4 has become the standard care for thyroid hormone replacement. It is customary to start with a low dose of 50 µg/d, increasing thereafter to 100 µg/d to 150 µg/d if required. At least six weeks should pass before repeating thyroid function tests and adjusting the dose, usually in increments of 25 µg/d.^[lxiv]
• Triiodothyronine/Liothyronine: A small subset of hypothyroid patients do not experience improvement in their symptoms with T4 monotherapy. In this instance, a combination of T4 and T3 hormone replacement therapy is preferred.^[lxv]

*Contact Metagenics Clinical Support to ensure product recommendations are suitable for use in conjunction with pharmaceutical medications.

Footnotes

References